And liver damage

TCDD is the most potent inducer of chloracne. This has been well known since the accident in Seveso, Italy, in 1976 in which large amounts of TCDD were distributed in the environment subsequent to an explosion in a factory that produced a chlorophenoxy herbicide, 2,4,5-T. TCDD is an impurity produced during the production of 2,4,5-T. The most common long-term effect of TCDD exposure was chloracne. Exposed individuals also suffered increased excretion of porphyrins, hyper-pigmentation, central nervous system effects, and liver damage and increased risk of cancer was a long-term consequence of the exposure. In addition to TCDD, polychlorinated biphenyls (PCBs), polychlorinated dibenzofurans, and polychloronaphthalens cause chloracne as well as other effects typical of TCDD. 7i... 

A Mutant Protein That Folds Slowly Can Cause Emphysema and Liver Damage... 

Pyridine may cause central nervous system depression, irritation of skin and respiratory tract Large doses may produce gastro-intestinal disturbances, kidney and liver damage (Refs 3 4)... 

Increased blood pressure No deaths Kidney damage Stomach and liver damage Liver and kidney damage Increased mortality... 

Increased respiration rate in 4 days, growth reduction and liver damage in 9 days, abnormal oocyte development and reduced spermatogonia production in 18-20 days 2... 

It was conclusively shown that deoxychlordiazepoxide (393) had none of the phototoxic properties of the parent drug, at least in the rat [225]. Chlordiazepoxide, demethylchlordiazepoxide, demoxepam and diazepam-4-oxide were all phototoxic to a bacterial cell preparation. There was a close relationship between the phototoxicities of the A-oxides and the toxicity in the dark of their oxaziridines. The reduced forms of the four compounds were not phototoxic [ 228 ]. Kinetic studies demonstrated that the oxaziridine (390) covalently bonds to plasma proteins. The half-life of the oxaziridine in the presence of high concentrations of protein was about 30 min. It therefore has time not only to bind to biomolecules in the skin surface, but also to attack internal organs. This was put forward as the explanation of previously observed kidney and liver damage in the rat [229]. 

Increase usually due to skeletal muscle, cardiac muscle, and liver damage. Not very specific unless isozymes are evaluated. 

At the initial stages of a release, when the benzene-derived compounds are present at their highest concentrations, acute toxic effects are more common than they are later. These noncarcinogenic effects include subtle changes in detoxifying enzymes and liver damage. Generally, the relative aquatic acute toxicity of petroleum will be the result of the fractional toxicities of the different hydrocarbons present in the aqueous phase. Tests indicate that naphthalene-derived chemicals have a similar effect. 

Symptoms of exposure Inhalation of vapors may cause drowsiness, incoordination, and liver damage. May irritate eyes and skin (Patnaik, 1992). An irritation concentration of 933.33 mg/m in air was reported by Ruth (1986). 

Symptoms of exposure May cause weakness, confusion, depression of central nervous system, dyspnea, weak pulse, and respiratory failure. May irritate eyes and mucous membranes. Contact with skin may cause burns and dermatitis. Chronic effects may include gastrointestinal disorders, nervous disorders, tremor, confusion, skin eruptions, oliguria, jaundice, and liver damage (NIOSH, 1997 Patnaik, 1992). 

Tables 1-1, 1-2, 1-3, and 1-4 show how little we know about the levels of 1,2-diphenylhydrazine that might affect your health. As is shown in Table 1-4, animals that ate food containing 1,2-diphenylhydrazine for a long time developed lung inflammation, stomach damage, and liver damage, and some died. Although the levels of exposure that cause harmful effects in humans are not known, as discussed in Section 1.2, 1,2-diphenylhydrazine is not likely to be found in food, and you are not even likely to be exposed to levels of concern if you live near a hazardous waste site. Additional information on levels of exposure associated with effects can he found in Chapter 2.

Breathing high levels of chromium (VI) can cause irritation to the nose, including nosebleeds, ulcers, and holes in the nasal septum. Ingesting large amounts of chromium (VI) can cause stomach upset and ulcers, convulsions, kidney and liver damage, and even death. Skin contact with certain chromium (VI) compounds can cause skin ulcers. Some people are extremely sensitive to... 

One company withdrew a niacin product it marketed because capsules contained 10 times the quantity of niacin claimed. Users experienced heart attacks, nausea and vomiting, and liver damage as a result of using the product. 

It is important to resolve whether primary structural damage in the liver causes subsequent lung and circulatory effects or whether primary pulmonary blockage is the cause of the circulatory effects and liver damage. 

Although unlikely in an occupational setting, ingestion of copper salts may cause vomiting, abdominal pain, diarrhea, lethargy, acute hemolytic anemia, renal and liver damage, neurotoxicity, increased blood pres-... 

Toxicology. Decalin is an irritant of the eyes and mucous membranes in animals it causes species- and sex-specific kidney and liver damage. 

Toxicology. Diphenylamine causes kidney and liver damage in animals. 

Guinea pigs exposed to 10 ppm for 2 hours exhibited immediate irritation of the eyes and nose a high percentage of the animals died, apparently from pneumonitis. In guinea pigs, the LCso for 8 hours was Img/m (0.3 ppm) pulmonary irritation and liver damage were observed. 

Toxicology. Methyl chloride is a central nervous system depressant it may cause kidney and liver damage, and it is a reproductive toxin and a teratogen in experimental animals. 

Toxicology. In animals, nitroethane is a respiratory irritant and, at high concentrations, it causes narcosis and liver damage methemo-globin has been reported after ingestion by humans. 

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